Sgt. Edward Conover, BA, SJPD
Mary Boudreau Conover BSNed
- Too much of a
good thing
- Other causes
of excited delirium
- The dope on dopamine
- Brain biomarkers
for excited delirium and sudden death
- Police action
- Time-line for
drug-related deaths during arrest or in-custody
- Complexity of
history taking
- Autopsy in excited
delirium
- The path to psychosis
and self-destruction
When police officers are called
out to subdue an aggressively violent individual who is destroying property
and is a serious physical threat to those in the vicinity, they respond
to the call knowing from the report that they may
encounter a case of excited delirium, a condition in which death is
imminent with or without police intervention, but all the same leaving
police officers vulnerable to lawsuit. This article has been sparked
and has taken life from the mortality review by Mash et al1
published by Forensic Science International in June 2009. The authors
of the landmark study, a group of scientists from Miami, Fl; Berkeley,
CA; Stockholm, Sweden; and Suffolk County, NY, showed that a 2-protein
biomarker signature, when combined with a description of the decedent’s
behavior prior to death, serves as a reliable forensic tool for an autopsy
identification of excited delirium, a syndrome known to be a terminal
event. The depth and breadth of the work involved is revealed in the
acknowledgment by the authors of the cooperation of the many physician
medical examiners and death investigators from throughout the United
States and Europe who are involved in medicolegal investigations of
excited delirium deaths. There were 90 cases studied, with 10 more added
since publication. The findings and on-going studies give hope to police
officers everywhere who are innocent targets when violently aggressive
cases of excited delirium die in custody.
TOO MUCH OF A GOOD THING
Fatal excited delirium is a
syndrome caused by the excessive chaotic signaling of dopamine, resulting
in death. Dopamine’s normal functions are to encourage and support
important roles in behavior including regulation of mood, memory, learning,
appetite, sleep, and muscle contractions. Dopamine occurs naturally
in the body and is released from the cerebral cortex to the frontal
lobes of the brain to help us concentrate, learn, form habits, and to
reward pleasurable experiences such as good food and sex so that we
will continue to pursue them in the interests of self-preservation,
social adaptation, learning, and meaningful progress along life’s
path.
Remember mom’s warning about
“too much of a good thing”? Mom knows. In the case of
dopamine, too much of this good thing will overtake you with craving,
drive you into a violent psychotic state, destroy you in every way possible,
and then eventually leave you to die in a fit of critically overheated
excited delirium after having lashed out with super-human strength to
destroy everyone and everything in the vicinity.
So, how does a person go about
getting too much of this good thing? It’s easy and it starts
with one “hit” with one of the stimulants of the central nervous
system (CNS) such as cocaine or methamphetamine.
OTHER CAUSES OF EXCITED
DELIRIUM
Delirium is a brain dysfunction
and clouding of consciousness that may be manifested with widely different
symptoms from somnolence to excited agitation, depending on the cause,
which includes the somnolent delirium of liver disease or the excited
delirium of mental stress, depression, suicidal tendencies, acute exhaustive
mania, underlying psychosis, alcohol withdrawal, or head trauma.2
3
Thus, illicit drugs are not
the only cause of excited delirium. The excited delirium manifested
in other conditions is sometimes referred to as “impulsive aggression”.
In such cases, laboratory tests show no trace of illicit drugs. Genetics
and hypofunction of the neurotransmitter, serotonin, have been implicated.4-7
Serotonin.
Serotonin is a neurotransmitter, as is dopamine. In the central
nervous system its functions include the regulation of mood, appetite,
sleep, muscle contraction, memory and learning. Disturbances of the
serotonin nerve pathway have been implicated in many psychiatric disorders,
including alcoholism, aggression, schizophrenia and depression.6
8 It has also been suggested that in such cases hypofunction of
serotonin may represent a biochemical trait that predisposes individuals
to impulsive aggression, with dopamine hyperfunction compounding the
serotonin deficit.4
Genetics.
Genetics and environment hold key roles in determining aggressive behavior.
In particular, reaction to stress appears to be an important
factor in precipitating such episodes and adverse rearing conditions
may interact with variants in stress and neurotransmitter pathway genes
leading to antisocial or violent behavior.9 Several
different genetic markers are thought to be associated with regulation
of mood, pain perception, aggression, and psychiatric disturbances such
as schizophrenia, depression, and suicide.5
Symptoms. Excited
delirium is recognized because of acute loss of behavioral inhibition
manifested in a cluster of behaviors that may include aggression, agitation,
ranting, hyperactivity, paranoia, panic, violence, public disturbance,
surprising physical strength, profuse sweating, hyperthermia, respiratory
arrest, and death. Knowing of the many and diverse causes of excited
delirium, it is not surprising that when a person exhibiting this hyperexcited
cluster of symptoms is subdued by the police, there may be no trace
of illicit drugs found in the blood sample taken in-hospital or at postmortem.
THE DOPE ON DOPAMINE
Dopamine is a neurotransmitter,
a chemical that carries messages from one nerve cell (neuron) to another.
Notice the two approximated neurons and the space between them in the
illustration below. This space is called a synapse. It
is here, in the synaptic gap that dopamine is released from the neuron
(nerve cell).
In
all cases of excited delirium and “impulsive aggression”, excessive
levels of dopamine in the extracellular fluid of the brain, although
they cannot be measured directly, are reflected in “dopamine
transporter levels that are below the range of values measured in
age-matched controls.”1 Once
dopamine has delivered its stimulus, it needs a transporter in order to
return into the neuron. The dopamine transporter is blocked by cocaine
and methamphetamine and eventually, with continued abuse of the drug,
the dopamine transporters fail, leaving unregulated dopamine to produce
the sudden unexpected onset of excited delirium.10 14
Cocaine in the Brain
The diagram below shows the sequence from 1-4 of normal activation of the nerve.1 11 12 13 When cocaine is aboard the normal physiology of dopamine is disrupted, as diagrammatically illustrated at #5.
Illustration adapted from the Nat Institute
on Drug Abuse Research Advances 13(2), 1998.
- Vesicles are shown
in their resting state, ready for the nerve to be activated. Dopamine rests within,
protected from destruction by the enzyme, monoamine oxidase.
- The nerve has been
activated and the vesicles quickly fuse with the cell membrane and unload the dopamine into the synaptic
space.
- The free dopamine diffuses to a receptor on the target neuron, binds, and releases
its charge.
- Dopamine then returns
to its dopamine-releasing reurons by binding to a site on its transporter, from wich it is transported across the cell membrane and delivered back to the vesicle.
- When cocaine is present, it binds to sites on the dopamine transporter, inhibiting uptake
of dopamine. Note dopamine cannot be reaccumulated and is literally
stranded. This represents an increase of dopamine levels in the brain which produce the rewarding and
reinforcing feelings of intense euphoria that, if pursued, may lead to addiction,
uncontrolled bingeing, and a path to death and destruction.
Methamphetamine14
Amphetamine and substituted
amphetamines, including methamphetamine (meth), methylphenidate (Ritalin),
methylenedioxymethamphetamine (ecstasy), and the herbs khat and ephedra,
are the only widely administered class of drugs that predominantly release
dopamine and norepinephrine from the nerve cell by a mechanism other
than their normal release from the vesicles. These drugs are used medicinally
and socially in many cultures, exert profound effects on mental function
and behavior, and can produce the degeneration of nerves and addiction.
Meth not only prevents the return transport of dopamine and norepinephrine
into the cell, it also works in two ways to increase the amount of dopamine
and norepinephrine for reverse transport out of the cell.
- Meth easily crosses
the blood/brain barrier and passes directly through the nerve cell membranes
into the nerve terminal to disrupt the normal functioning of the CNS
stimulants, dopamine and norepinephrine.
- Once inside the
cell, meth causes dopamine and norepinephrine to be released from the
vesicles where they are stored, and then transports them out of the
cell, using their uptake carriers in. a reverse direction.
- It binds to the
dopamine and norepinephrine transporters, preventing return of these
neurotransmitters back into the nerve cell and thus increasing their
concentration in the synapse.
- Meth also blunts
the effects of an enzyme in the intracellular fluid (monoamine oxidase)
whose job it is to reduce concentrations of dopamine and norepinephrine.
An attempt to adapt.
As more and more dopamine transporters are being used up by cocaine
or meth, the body adapts by increasing the numbers and function of the
dopamine transporter. When this adaptation fails, dopamine transporter
levels fall and dopamine itself is no longer regulated, triggering a
sudden and potentially fatal bout of excited delirium.1 15 16
BRAIN BIOMARKERS FOR EXCITED
DELIRIUM AND SUDDEN DEATH
Neurochemical Pathology
Findings. For police officers everywhere, support and validation
can be found in the eloquent studies of Mash et al1 at the
Department of Neurology at the University of Miami (www.exciteddelerium.org).1a This group has
conducted a mortality review of ninety excited delirium deaths.
Their findings implicate central nervous system dysfunction involving
the neurotransmitter dopamine as the cause of the excited delirium.
The fatal event for most is hyperthermia; for all it is collapse of
the autonomic nervous system. Important findings at autopsy were:
Core temperature. Measured
at autopsy, possibly after a cool-down, mean core body temperature was
has been 105.2 degrees F (40.7 degrees C) in cocaine abusers and cases
of exhaustive mania.
2-protein biomarker (dopamine
transporter and heat shock protein) analysis.
- Heat shock protein
elevation. Heat shock protein (Hsp70) was elevated up to 4-fold
in the postmortem brain, confirming that hyperthermia is an associated
symptom and often a harbinger of death. Heat shock proteins increase
their expression in cells with elevated temperatures. They are thought
to be defense mechanisms or neuroprotective whenever core body temperature
is elevated. This marker is a surrogate for hyperthermia in cases of
excited delirium.
- Dopamine transporter
blood levels. Low levels are a positive finding for excited
delirium. Toxicology and history of drug or alcohol abuse or a
psychological autopsy will help to show cause.
Mash and her associates1
have concluded after review of chemical pathology and toxicology results
from a case series of 90 excited delirium deaths, that the identification
of postmortem biomarkers for excited delirium serve as an objective-testing
method for assisting medical examiners at autopsy. The use
of postmortem biomarkers when combined with descriptions of the decedent’s
behavior prior to death, are reliably associated with the syndrome.
POLICE ACTION
Arriving on scene, police often
find the individual involved in dangerous behavior---assaulting friends,
family and total strangers, destroying property, running wildly in and
out of traffic, throwing off their clothes, kicking in doors, invading
homes, and breaking windows.1
This frightening scenario is
indeed a challenge to the police who, though strong, do not have the
“unexpected superhuman physical strength” of excited delirium. Added
to the quagmire is the fact that the combative person is impervious
to pain and is unable to respond to verbal commands. The usual police
techniques of pain control are useless and it often takes many police
officers to control the suspect. Should there be a high intensity physical
struggle, vital signs are often lost within minutes of being restrained.1
In the midst of this maelstrom
and under extreme psychological and time pressures, the officers need
to choose the most appropriate force option available to them at the
time that balances the safety of the public, the officers and the suspect.
However, even careful use of the options available followed by immediate
medical attention does not guarantee survival. In this chemically altered
physical condition, it is possible, even with extreme care, that the
suspect will die suddenly while being restrained in police custody,
especially if a protracted physical struggle is necessary. Ideally,
the police officers need to incapacitate the individual as quickly as
possible, for the good of the suspect and those endangered by his violence.
The longer the fight continues, the worse the outcome for the suspect,
especially if the combative person is under the influence of phencyclidine
(PCP) or central nervous system (CNS) stimulants such as methamphetamine
(meth), amphetamine, or cocaine ("crack"). These stimulants
have profound chemical effects on the heart and brain, causing abnormal
brain activity which can lead to excited delirium and sudden death.1 Should
the suspect be successfully resuscitated, they often die in-hospital
from rhabdomyolysis and renal failure.17 18
The cause of
death in excited delirium is a gross disruption of the central nervous
system causing symptoms that produce very high body temperatures, multisystem
organ failure, and death. In such a rapidly declining physical and mental
state, case reviews have demonstrated the high risk of mortality for
these individuals---all on their own without police intervention.17
19
Avoiding a Potentially
Fatal Struggle
Electrical devices.
In the past the fastest way to quickly incapacitate the suspect was
the carotid restraint. More recently, there is widespread availability
of electrical devices that conduct just enough energy to subdue a violent,
out-of-control suspect who is impervious to pain and unable to understand
police commands. TASER is the most well known manufacturer of such a
device and has become the more common force response.
There is a significant difference
between the Taser and the ‘stun gun’. The Taser causes Electro Muscular
Disruption (EMD) which actually disrupts the muscles and causes involuntary
immobilization. The Stun Gun is a Conductive Energy Device that delivers
a shock, which is a pain compliance type issue. When hit with a ‘stun
gun’ a person with excited delirium can fight through the pain. Whereas,
when the Taser works properly, they have no choice in the matter, the
pain is secondary and voluntary control of skeletal muscles is disrupted,
during which time police can restrain the suspect.
The Taser has come under scrutiny
by national and international media and human rights organizations because
there have been deaths of persons in custody following its application.
Current theories include production of immediate fatal arrhythmias or
“some type” of subacute, delayed cardiac or other organ system damage
that manifests itself as sudden death at a later time.20
Such opinions have elicited
scientific investigations demonstrating that prolonged EMD application
in exhausted humans did not cause arrhythmias nor was there a detectable
change in their 12-lead ECGs.21 In another study of a resting
adult population, for a 24-hour period after a 5-second application
of the Taser, the ECG was unaffected, nor were arrhythmias or significant
direct cardiac cellular damage that may be related to sudden and unexpected
death detected. No evidence of dangerous hyperkalemia , induced acidosis,
or an increase in core body temperature was found.22
23 Regarding the human stress response, Dawes, et al
have shown that the EMD or other electrical devices do not elicit this
response any more than other uses of force and are safer than a prolonged
physical struggle for the person in excited delirium.24 These
investigators were affiliated with:
- Department of Emergency
Medicine, Hennepin County Medical Center, Minneapolis, MN
- Department of Cardiology,
Cleveland Clinic and Hospital, Cleveland, OH.22
- Emergency Department,
Lompoc District Hospital, Lompoc, CA
- Department of Emergency
Medicine, Hennepin County Medical Center, Minneapolis, MN
- Division of Medical
and Technical Research, Taser International, Inc., Scottsdale, AZ
- Emergency Department,
Meridian Park Hospital, Tualatin, OR23
- Lompoc Valley Medical
Center, Lompoc, CA24
- Hennepin County
Medical Center, Minneapolis, MN24
Carotid restraint. The
carotid restraint used in law enforcement to subdue people with excited
delirium has its origin in Jiu-Jitsu---the technique is the same. Although
this restraint is sometimes referred to as “the choke hold”, it
does not place pressure over the trachea with the intention of cutting
off air; it is not a choking hold. The misnomer is unfortunate and misleading
for the public and in a court of law. Correctly applied, the trachea
lies protected in the bend in the officer’s arm while pressure is
applied over the two carotid arteries on the sides of the neck, causing
the suspect to lose consciousness. This short period of unconsciousness
can be used by officers to take the suspect into custody.
Transport of the prisoner.
Violently agitated prisoners should always be taken to a hospital, never
to a jail, and they should not be transported in a police car. Whatever
the means of transport, victims need close supervision.
Summary.
For all police officers, the use or Taser or carotid restraint on an
agitated, violently combative person is an attempt to quickly
gain control and avoid a prolonged and potentially dangerous life-threatening
struggle for a person who is psychotic, unable to process verbal police
instructions, and physically unfit for a struggle, something that he
is unable to comprehend.
TIME-LINE
FOR DRUG-RELATED DEATHS DURING ARREST OR IN CUSTODY
Stephen. B. Karach, M.D. and
Boyd. J. Stephens, M.D.25 report that remedies to treat cases
of excited delirium are currently ineffective and survival is unlikely.
This is as opposed to prevention of death in drug withdrawal, suicide,
and natural causes. As Drs. Karach and Stephens have pointed,
out this critical difference places drug related deaths in a different
category, requiring that they be considered separately.
Time of Drug-Related Deaths
in Prisoners Related to Cause
The cause of drug-related deaths
in prisoners usually fall into four time periods: during arrest, 2 hours
later, within 12 hours, and after 12 hours.26
- During arrest and
transport, excited delirium is the principal cause of death and drug
dealers swallowing the evidence at the time of arrest being another.
- Approximately 2
hours after arrest rhabdomyolysis and multisystem failure are the causes
of death..
- Within 12 hours
of arrest, death is usually from massive overdose in smugglers and dealers.
- After 12 hours but
while still on remand—most often deaths are related to withdrawal
or natural causes.
In some cases, death occurs
at home, unattended. In one study, investigators at the scenes
found the person dead with elevated rectal temperatures, abrasions on
the extremities, and damaged and tossed dwellings. Positive toxicology
confirmed drug-induced excited delirium.1 More often,
police are summoned during the psychotic agitation phase. Taser deployment
is used to quickly subdue and restrain the victim, avoiding a prolonged
struggle involving the efforts of five or six officers or use of chemical
agents which usually have no effect.25
Most, but not all, victims
of excited delirium are chronic, long-term, high-dose CNS stimulant
abusers. Initially hyperthermic, they soon become psychotic, experiencing
several hours of violent agitation followed by cardiac arrest a few
hours later, with or without police intervention. Even when medical
intervention is immediately available and without the stress of restraint,
there is still a high risk of death.17 If attempts at resuscitation
are successful, almost all victims die of rhabdomyolysis and multisystem
failure a few days later.1 25- 27
Rhabdomyolysis
Rhabdomyolysis is a well-documented
complication of cocaine and other illicit drugs because of the extremely
intense and violent muscle activity involved. It has been reported
in 24% of cocaine users.37 In fact, Ruttenber, et al17 have
concluded that “because cocaine-associated rhabdomyolysis and excited
delirium have similar clinical features and risk factors, occur in similar
populations of drug users, and can be explained by the same pathophysiologic
processes”, they are different stages of the same syndrome and are
caused by changes in dopamine processing induced by chronic and intense
use of cocaine rather than by the acute toxic effects of the drug.17
COMPLEXITY OF HISTORY TAKING
Tanquay, et al28
relate an unusual case in which a man died suddenly while running naked
on the street. The initial death investigation listed excited
delirium from drug intoxication, which would have compounded the sorrow
for his family. Autopsy revealed obstruction of breathing by an
inflammatory laryngeal polyp. Toxicology studies were negative and investigation
revealed a visit at a hospital the day before his death when he was
complaining of stridor (difficult breathing). He sought help and
found none. It is believed he developed airway obstruction while
dressing at home, couldn’t breathe, and ran out on the street desperate
to find help.
Dr. Tanquay’s case is admittedly
unusual. It does, however, impresses one with the importance of
a thorough death investigation, especially when that death was a sudden
psychiatric death while in police custody. Police officers must
realize that although sudden death in the context of excited delirium
is not unexpected, the interest and influence of an uninformed media
and possible witnesses requires a complex police investigation, including
the personal, social, and business milieu in the decedent’s life that
would not ordinarily be part of a postmortem police investigation. The
complexity of aggression sends the investigation deep into the personal
life of the decedent. You are looking for signs of stress, medical
problems, aberrant behavior, history of abuse, etc. There is much at
stake. The investigation should include:
- Description of the
scene and circumstances surrounding the death
- Review of records
from emergency departments
- Complete autopsy
- Toxicologic analysis
of cocaine and other licit or illicit drugs in the blood
- Personal history
- Reports from social
contacts (attitudes, stress, angry outbursts, etc.)
- Medical history
- Recent increases
of stress (financial, domestic, personal)
- Prior incidents
of aggression
- Activities and situations
immediately prior to the violent incident
- Complaints of poor
health or unusual symptoms prior to the sudden onset of excited delirium
- Compliancy in taking
prescribed medications
- Evidence of adverse
rearing conditions
Police officers are referred
for more information on history taking to:
http://policechiefmagazine.org/magazine/index.cfm?fuseaction=display_arch&article_id=191&issue_id=12004
AUTOPSY FINDINGS IN EXCITED
DELIRIUM
The importance of the findings
at autopsy cannot be over estimated. If death occurs while officers
are trying to restrain a victim, the police may be assumed to be responsible
simply on the basis of proximity. If the case comes to legal review,
the issues raised are predictable, thus, everything should be done to
ensure well documented events and findings.25
Core body temperature: A
body temperature greater than or equal to 103º F (39.44º C) is considered
to be evidence of hyperthermia. A rectal temperature should be taken as soon as qualified medical staff can do so on a suspect admitted
to hospital after such an incident or by the coroner in the case no
temperature was obtained prior to death. Ear canal infrared measurement,
skin strips, and skin palpations should be avoided, as they are unreliable.1
Drug levels in the blood.
Illicit drugs in the blood obviously confirms that the decedent used
drugs, although a negative report does not prove absence of excited
delirium. Brain toxicology is a preferred matrix, since many abused
substances can be detected over longer periods.1
2-protein biomarker (dopamine
transporter and heat shock protein) analysis
- Dopamine transporter
blood levels. Low levels are a positive finding for excited
delirium, Toxicology and history of drug or alcohol abuse or a
psychological autopsy will help to show cause.
- Heat shock protein
(Hsp70). Elevated whenever core body temperature is increased.
This marker is a surrogate for hyperthermia in cases of excited delirium.
Markers for intravenous
drug abuse. These may also be present, but their presence
only provides confirmatory evidence of chronic drug abuse.30 31
Cocaine concentrations
in blood and brain. Levels will be modest, but concentrations
of the cocaine metabolite benzoylecgonine may be quite high because
of its longer half-life32 and it accumulates in the tissues
of chronic users.28
Test for chemical agents,
particularly capsicum spray. Karch and Stephens25
state that in their experience these agents have no effect on patients
with excited delirium, but that if the victim dies, death will be blamed
on their use. Failure to recover the sprayed capsicum from the
facial area, or from the airway in cases of accidental death, is reasonable
evidence that capsicum did not enter the lungs and did not directly
cause toxicity or death. Methanolic swabs (saline swabs in the
living) can be used to recover capsicum from the skin and clothing.
Of course, if capsicum is not a factor, death cannot be attributed to
its use.
Pulse oximetry monitoring.
Accusations of positional asphyxia can be precluded in this way. If
vital signs and oxygen saturation are continuously recorded during transport,
then it matters little what position the decedent was in or how he was
restrained, provided it can be proven that his respiratory status was
not impaired.
Temperature.
The victim’s temperature is recorded as soon as possible. Although
this is rarely done with an agitated person, without documentation of
hyperthermia, it becomes more problematic to prove excited delirium.
If the victim cannot be resuscitated, rectal temperature should be recorded
as soon after death as possible, and again at autopsy.
Photograph.
The victim is photographed to document both the absence of and the presence
of petechiae or bruises. Petechiae can form after death.
If their absence is not documented, and they are found during a second
autopsy charges of incompetence or cover-up may result.
Brain dopamine and kappa
receptors. To document these changes, the brain is removed
and frozen within 12 hours. Frozen samples can then be sent to a reference
neurochemistry laboratory.28
Traumatic injury to the
neck. The thoracic organs and the brain should be removed
before the neck dissection to decompress venous return and prevent artifactual
bleeding into the soft tissues of the neck, the presence of which may
falsely suggest traumatic injury. Obviously, a scrupulous well-photographed
neck dissection will be required to determine whether a choke hold or
neck compression has been applied.33
Heart examination. Careful
weighing, measurement of wall thickness, and the taking of multiple
sections for histological examination are important.34
Since heart size is an independent risk factor for sudden death,35
the measurement may prove to be a very significant factor in determining
the cause of death.
Autopsy report on a case
of non-drug related excited delirium. Bunai et al36
the arrest and death in Japan of a
39-year-old man suspected of being a rapist. He “vigorously resisted”
arrest, but was eventually restrained after a 20-minute struggle with
police officers and several men. He collapsed shortly thereafter, was
transported to a hospital, and pronounced dead on arrival. His rectal
temperature was 40 degrees C. (104 degrees F) 2.5 hours after death.
Autopsy revealed abrasions and subcutaneous hemorrhages of the head,
face, arms, and legs. The heart was dilated and there were subendocardial
hemorrhages in the left ventricle. The brain and both lungs were congested.
Microscopic examination of the lungs revealed intra-alveolar edema and
hemorrhages. The skeletal muscles showed contraction band necrosis and
hyaline degeneration. The liver showed diffuse coarse-droplet fatty
infiltration of hepatocytes. Neither addictive drugs nor alcohol were
detected from the blood or urine. It was concluded that cause of death
was fatal hyperthermia in a state of excited delirium.
A PATH
TO PSYCHOSIS AND SELF-DESTRUCTION13
First use.
At low oral doses of CNS stimulants, alertness is improved; mood is
elevated, sexual arousal intensifies and appetite is suppressed.
Pupils dilate; heart rate and blood pressure increase.
Triggers.
After this the budding drug addict is at the mercy of internal and external
triggers such as a person, place, or thing associated with using.
Internal triggers are often emotional such as anger, desire, hurt, or
fear. The triggers can lead to the thought about using. If the
person does not block the thought or leave the triggering situation,
an escalating intense craving takes control and the victim will stop
at nothing to have the drug.
At higher
doses. Acute intoxication of the CNS occurs, especially after
intravenous use. The effects are intense, distracting, and overwhelming.
The person is exhilarated and euphoric with feelings of great physical
strength and mental capacity, excitation, panic, and sexual arousal.
In some cases even when it is the initial CNS intoxication, the person
may have hallucinations, delusions and combative behavior.
Tweaking
phase. Then enters the phase known as “tweaking”. During
this phase, euphoria is gradually replaced with mounting anxiety, irritability,
delusions, paranoia, and pseudo-hallucinations. Binging continues
in pursuit of the initial “upside”, but the highs collapse into
deeper lows leading to exhaustion---the onset of the “crash phase.”
Crash phase.
At this point the user stops administration of the drug and sleeps
restlessly for a day or more.
Psychotic
phase. Continued binge-type drug use brings true schizophrenic-like
hallucinations, delusions, and over-heated, violent behavior.
Most are chronic freebase “crack” cocaine users who have recently
been on a binge. This excited delirium phase is often a terminal
event, with death occurring
within hours of the onset of symptoms, alone or in police custody.
ACKNOWLEDGEMENTS
We are grateful to Deborah
C. Mash Ph.D. for her review of the section on “Brain biomarkers
for excited delirium and sudden death. Dr. Mash is
Professor of Neurology and Molecular and Cellular Pharmacology, Jeanne
C Levey Chair for Parkinson's Disease Research, Dept. of Neurology,
Miller School of Medicine, University of Miami, Florida. Co-authors
with Deborah C Mash Ph.D on this study were:
- Linda Duque,
CAP; John Pablo, PhD; Yujing Qin, PhD; Nikhil Adi, PhD, Dept.
of Neurology, Miller School of Medicine, University of Miami, FL.
- W. Lee Hearn,
M.D. and Bruce A. Hyma, M.D. Miami-Dade Medical Examiner Dept.,
Miami, FL.
- Steven B. Karch,
MD, FFFLM, Consultant Cardiac Pathologist & Toxicologist, Berkeley,
CA.
- Henrik Druid,
M.D., PhD, Dept.of Forensic Medicine, Karolinska Institute, Stockholm,
Sweden.
- Charles V. Wetli,
M.D., Dept. of Health Services, Division of Medical Legal Investigations
and Forensic Sciences, Suffolk County, NY.
- We would also like to thank
David Sulzer, Ph.D, for his careful review of the section on neurophysiology
and the effect of methamphetamine and cocaine. Dr. Sulzer is Associate
Professor of Clinical Psychiatry and Neuroscience at Columbia University,
NYC, NY with an area of research that includes synapes and circuits,
neurodegeneration and repair. He specializes in neurotransmission
and mechanisms of neurodegeneration in basal ganglia and dopamine neurons.
Thank you, David; your review and changes were greatly appreciated.
REFERENCES
1. Mash DC, Duque L, Pablo
J, Oin Y, Adi N, Hearn WL, Hymab BA, Karch SB, Druid H, Wetli CV:
Brain biomarkers for identifying excited delirium as a cause of sudden
death. Forensic Science International 190 (2009) e13–e19.
1a. Excited delerium, education,
research information. www.exciteddelerium.org
2. Ross CA, Peyser CE, Shapiro
I, Folstein MF: Delirium: phenomenologic and etiologic subtypes.
Int Psychogeriatr. 1991 Winter;3(2):135-47.
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